Am J Physiol Cell Physiol Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol 253: C193-C198, 1987;
0363-6143/87 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Weissberg, P. L.
Right arrow Articles by Bobik, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Weissberg, P. L.
Right arrow Articles by Bobik, A.

AJP - Cell Physiology, Vol 253, Issue 2 C193-C198, Copyright © 1987 by American Physiological Society

ARTICLES

Na-H antiport in cultured rat aortic smooth muscle: its role in cytoplasmic pH regulation

P. L. Weissberg, P. J. Little, E. J. Cragoe Jr and A. Bobik

We have investigated the role of the Na-H antiport in the regulation of intracellular pH (pHi) in vascular smooth muscle. Experiments were conducted on contractile-state rat aortic smooth muscle cells grown in primary culture and loaded with the pH-sensitive, fluorescent indicator 2',7',-biscarboxyethyl-5(6)-carboxyfluorescein (BCECF). Cells equilibrated in a normal physiological salt solution (PSS) containing 135 mM Na, pH 7.4 at 37 degrees C, had a pHi of 7.16 +/- 0.04 (means +/- SE; n = 8). 5-(N-ethyl-N-isopropyl)amiloride (EIPA) caused a concentration-dependent fall in pHi. Removal of extracellular Na caused an intracellular acidification that was rapidly reversed on replacement of Na. The rate of recovery from NH4Cl-induced intracellular acidosis was dependent on extracellular Na concentration (Km 14.6 +/- 2.8 mM) and was accelerated by increasing the transmembrane Na gradient and slowed by decreasing it. Recovery from acidosis was completely abolished by either EIPA or the absence of extracellular Na. These results demonstrate that the Na-H antiport is an important mechanism for the maintenance and regulation of pHi in vascular smooth muscle cells. The BCECF fluorescence technique provides an ideal method for further studies on the mechanisms for pHi regulation in these cells.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Renal Physiol.Home page
A. A. Banday and M. F. Lokhandwala
Oxidative stress-induced renal angiotensin AT1 receptor upregulation causes increased stimulation of sodium transporters and hypertension
Am J Physiol Renal Physiol, September 1, 2008; 295(3): F698 - F706.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
K. Jandeleit-Dahm, K. M. Hannan, C. A. Farrelly, T. J. Allen, J. R. Rumble, R. E. Gilbert, M. E. Cooper, and P. J. Little
Diabetes-Induced Vascular Hypertrophy Is Accompanied by Activation of Na+-H+ Exchange and Prevented by Na+-H+ Exchange Inhibition
Circ. Res., December 8, 2000; 87(12): 1133 - 1140.
[Abstract] [Full Text] [PDF]

Home page
 J. Pharmacol. Exp. Ther.Home page
D. Haikerwal, A. M. Dart, P. J. Little, and D. M. Kaye
Identification of a Novel, Inhibitory Action of Amiodarone on Vesicular Monoamine Transport
J. Pharmacol. Exp. Ther., February 1, 1999; 288(2): 834 - 837.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online